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Impact of trans‐fatty acid sources on the fetal programming of atherosclerosis
Author(s) -
Gates Louise J,
Kraft Jana,
LangleyEvans Simon C,
Lock Adam L,
Salter Andrew M
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.990.2
Subject(s) - offspring , endocrinology , medicine , pregnancy , cholesterol , biology , gestation , adipose tissue , fetus , genetics
Increasing evidence suggests that perturbations in maternal diet can impact the susceptibility of offspring to atherosclerotic vascular disease. The aim of this study was to elucidate effects of maternal intake of different sources of trans ‐fatty acids (TFA) namely, partially hydrogenated vegetable oil (PHVO) and butter oil (BO) produced from TFA‐enriched cow's milk on the development of atherosclerosis (ATH) in their offspring using the ATH‐susceptible ApoE*3 Leiden mouse (AEL). Female wild type C57BL/J6 mice were mated with heterozygous AEL males and fed diets supplemented with 13% either PHVO or BO. The fat sources were matched for total TFA (PHVO 16.5g; BO 16.9g/100g fat) but differed in TFA isomer profile. At birth dams were transferred onto a chow diet and female AEL offspring were subsequently weaned onto either a chow or atherogenic diet (13% cocoa butter, 0.2% cholesterol) for 12 wks. Plasma lipids, triaclyglycerides, and cholesterol correlated with ATH outcome (p<0.001); maternal diet however, had no significant impact on plasma cholesterol or triacylglycerol of the offspring. Histological analysis of sections through the aorta showed that offspring fed the atherogenic diet had more lesions than those fed chow (p<0.0001), but there was no difference between the offspring of dams fed the TFA sources. Offspring of dams fed BO had larger abdominal adipose tissue depots (p=0.059). In conclusion, the source of TFA within the maternal diet during gestation did not impact offspring's susceptibility to atherosclerosis.